ArticleInternational journal of molecular medicine2026
Recombinant myonectin ameliorates sepsis‑induced cardiomyopathy by alleviating mitochondrial dysfunction via the AdipoR1/AMPK pathway.
Article in International journal of molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sepsis‑induced cardiomyopathy (SIC) is a common complication of sepsis and is associated with a high mortality rate; however, effective therapies remain lacking. Mitochondrial dysfunction is a key pathogenic mechanism. Myonectin, also known as C1q tumor necrosis factor‑related protein 15, is a novel member of the C1q/TNF‑related protein family. It has been demonstrated to exert cardioprotective effects by suppressing inflammatory response, inhibiting apoptosis and attenuating cardiac fibrosis. Despite these known functions, whether myonectin protects against SIC remains unclear. The present study aimed to investigate the protective potential of recombinant myonectin (rMyonectin) against SIC. Lipopolysaccharide (LPS)‑induced and cecal ligation and puncture‑induced SIC models were established in C57BL/6J mice, and LPS‑stimulated neonatal mouse cardiomyocytes (NMCMs) were used for
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